Skip to main content
eScholarship
Open Access Publications from the University of California

Hipk2 cooperates with p53 to suppress γ-ray radiation-induced mouse thymic lymphoma.

  • Author(s): Mao, J-H
  • Wu, D
  • Kim, I-J
  • Kang, HC
  • Wei, G
  • Climent, J
  • Kumar, A
  • Pelorosso, FG
  • DelRosario, R
  • Huang, EJ
  • Balmain, A
  • et al.
Abstract

A genome-wide screen for genetic alterations in radiation-induced thymic lymphomas generated from p53+/- and p53-/- mice showed frequent loss of heterozygosity (LOH) on chromosome 6. Fine mapping of these LOH regions revealed three non-overlapping regions, one of which was refined to a 0.2 Mb interval that contained only the gene encoding homeobox-interacting protein kinase 2 (Hipk2). More than 30% of radiation-induced tumors from both p53+/- and p53-/- mice showed heterozygous loss of one Hipk2 allele. Mice carrying a single inactive allele of Hipk2 in the germline were susceptible to induction of tumors by γ-radiation, but most tumors retained and expressed the wild-type allele, suggesting that Hipk2 is a haploinsufficient tumor suppressor gene for mouse lymphoma development. Heterozygous loss of both Hipk2 and p53 confers strong sensitization to radiation-induced lymphoma. We conclude that Hipk2 is a haploinsufficient lymphoma suppressor gene.

Many UC-authored scholarly publications are freely available on this site because of the UC's open access policies. Let us know how this access is important for you.

Main Content
Current View